PMID- 11119517
OWN - NLM
STAT- MEDLINE
DCOM- 20010118
LR  - 20240509
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 69
IP  - 1
DP  - 2001 Jan
TI  - Modulation of human immune response by Echinococcus granulosus antigen B and its 
      possible role in evading host defenses.
PG  - 288-96
AB  - By directly suppressing the function of certain immune cell subsets and by 
      stimulating other cell populations related to immunopathology, parasite-derived 
      substances play an important role in the chronic establishment of parasitic 
      disease. Our objective was twofold: (i) to investigate further the role of 
      Echinococcus granulosus antigen B (AgB) in the human early inflammatory response 
      by determining its effect on polymorphonuclear cell (PMN) random migration, 
      chemotaxis, and oxidative metabolism and (ii) to determine its action in acquired 
      immunity by evaluating AgB and sheep hydatid fluid (SHF)-driven Th1 (gamma 
      interferon [IFN-gamma] and interleukin 12 [IL-12]) and Th2 (IL-4 and IL-13) 
      cytokine production by peripheral blood mononuclear cells (PBMC) from 40 patients 
      who had cured or stable or progressive cystic echinococcosis. AgB significantly 
      inhibited PMN recruitment but left their random migration and oxidative 
      metabolism unchanged. Patients' PBMC stimulated with AgB produced IL-4 and IL-13 
      but did not produce IL-12. They also produced significantly lower IFN-gamma 
      concentrations than did PBMC stimulated with SHF (P = 10(-5)). AgB skewed the 
      Th1/Th2 cytokine ratios towards a preferentially immunopathology-associated Th2 
      polarization, predominantly in patients with progressive disease. AgB-stimulated 
      patients' PBMC also proliferated less than SHF-stimulated PBMC (P = 9 x 10(-3)). 
      In vitro Th2 cytokine production was reflected in vivo by elevated specific 
      immunoglobulin E (IgE) and IgG4 antibodies binding to AgB. These findings confirm 
      that AgB plays a role in the escape from early immunity by inhibiting PMN 
      chemotaxis. They also add new information on the host-parasite relationship, 
      suggesting that AgB exploits the activation of T helper cells by eliciting a 
      nonprotective Th2 cell response.
FAU - Rigano, R
AU  - Rigano R
AD  - Department of Immunology, Istituto Superiore di Sanita, Rome, Italy.
FAU - Profumo, E
AU  - Profumo E
FAU - Bruschi, F
AU  - Bruschi F
FAU - Carulli, G
AU  - Carulli G
FAU - Azzara, A
AU  - Azzara A
FAU - Ioppolo, S
AU  - Ioppolo S
FAU - Buttari, B
AU  - Buttari B
FAU - Ortona, E
AU  - Ortona E
FAU - Margutti, P
AU  - Margutti P
FAU - Teggi, A
AU  - Teggi A
FAU - Siracusano, A
AU  - Siracusano A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Antibodies, Helminth)
RN  - 0 (Antigens, Helminth)
RN  - 0 (Cytokines)
RN  - 11062-77-4 (Superoxides)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Animals
MH  - Antibodies, Helminth/biosynthesis
MH  - Antigens, Helminth/*immunology
MH  - Cytokines/biosynthesis
MH  - Echinococcus/*immunology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Humans
MH  - Interleukin-12/biosynthesis
MH  - Lymphocyte Activation
MH  - Male
MH  - Middle Aged
MH  - Neutrophils/physiology
MH  - Sheep
MH  - Superoxides/metabolism
MH  - T-Lymphocytes/immunology
PMC - PMC97883
EDAT- 2000/12/19 11:00
MHDA- 2001/02/28 10:01
PMCR- 2001/01/01
CRDT- 2000/12/19 11:00
PHST- 2000/12/19 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/12/19 11:00 [entrez]
PHST- 2001/01/01 00:00 [pmc-release]
AID - 1038 [pii]
AID - 10.1128/IAI.69.1.288-296.2001 [doi]
PST - ppublish
SO  - Infect Immun. 2001 Jan;69(1):288-96. doi: 10.1128/IAI.69.1.288-296.2001.